Evidence map›Paper›PMID 27302171›Full record

ArticleCancer research2016

HOXC10 Expression Supports the Development of Chemotherapy Resistance by Fine Tuning DNA Repair in Breast Cancer Cells.

Helen Sadik, Preethi Korangath, Nguyen K Nguyen, Balazs Gyorffy, Rakesh Kumar, Mohammad Hedayati, Wei Wen Teo, Sunju Park, Hardik Panday, Teresa Gonzalez Munoz and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  6. Review
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  8. Review
  9. Article
  10. The expression ofAnnals of translational medicine · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Role of HOXC10 in Cancer.Frontiers in oncology · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 1 institution in 1 country.

Helen SadikDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Preethi KorangathDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Nguyen K NguyenDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Balazs GyorffyMTA TTK Lendület Cancer Biomarker Research Group, Budapest, Hungary. 2nd Department of Pediatrics, Semmelweis University, Budapest, Hungary.
Rakesh KumarDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas.
Mohammad HedayatiDepartment of Radiation Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Wei Wen TeoDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Sunju ParkDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Hardik PandayDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Teresa Gonzalez MunozDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Otilia MenyhartMTA TTK Lendület Cancer Biomarker Research Group, Budapest, Hungary. 2nd Department of Pediatrics, Semmelweis University, Budapest, Hungary.
Nilay ShahDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Raj K PanditaDepartment of Radiation Oncology, The Houston Methodist Research Institute, Houston, Texas.
Jenny C ChangMethodist Cancer Center, The Houston Methodist Research Institute, Houston, Texas.
Theodore DeWeeseDepartment of Radiation Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Howard Y ChangHoward Hughes Medical Institute, Stanford University School of Medicine, Stanford, California.
Tej K PanditaDepartment of Radiation Oncology, The Houston Methodist Research Institute, Houston, Texas. saras@jhmi.edu tpandita@houstonmethodist.org.
Saraswati SukumarDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland. saras@jhmi.edu tpandita@houstonmethodist.org.
Semmelweis University · HU

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
CHROMATIN MODIFYING FACTORS CONTROL RADIATION RESPONSE AND GENOMIC STABILITYR01CA129537 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2008 to 2018
$3.3M
Tumor-cell-specific targets for combined hyperthermia and radiation effectsR01CA154320 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI PANDITA, TEJ K · 2010 to 2014
$1.6M
Functional Characterization of the Mammalian MOF Gene ProductR01CA123232 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2007 to 2011
$1.5M
Role of Heterochromatin protein 1 Beta in Genome Maintenance and OncogenesisR01GM109768 · NIGMS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI PANDITA, TEJ K · 2014 to 2017
$1.2M
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA088843NCI NIH HHS R01 CA123232NCI NIH HHS R01 CA129537NCI NIH HHS R01 CA154320NIGMS NIH HHS R01 GM109768NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

Development of drug resistance is a major factor limiting the continued success of cancer chemotherapy. To overcome drug resistance, understanding the underlying mechanism(s) is essential. We found that HOXC10 is overexpressed in primary carcinomas of the breast, and even more significantly in distant metastasis arising after failed chemotherapy. High HOXC10 expression correlates with shorter recurrence-free and overall survival in patients with estrogen receptor-negative breast cancer undergoing chemotherapy. We found that HOXC10 promotes survival in cells treated with doxorubicin, paclitaxel, or carboplatin by suppressing apoptosis and upregulating NF-κB Overexpressed HOXC10 increases S-phase-specific DNA damage repair by homologous recombination (HR) and checkpoint recovery in cells at three important phases. For double-strand break repair, HOXC10 recruits HR proteins at sites of DNA damage. It enhances resection and lastly, it resolves stalled replication forks, leading to initiation of DNA replication following DNA damage. We show that HOXC10 facilitates, but is not directly involved in DNA damage repair mediated by HR. HOXC10 achieves integration of these functions by binding to, and activating cyclin-dependent kinase, CDK7, which regulates transcription by phosphorylating the carboxy-terminal domain of RNA polymerase II. Consistent with these findings, inhibitors of CDK7 reverse HOXC10-mediated drug resistance in cultured cells. Blocking HOXC10 function, therefore, presents a promising new strategy to overcome chemotherapy resistance in breast cancer. Cancer Res; 76(15); 4443-56. ©2016 AACR.

Indexed as

Breast NeoplasmsDNA RepairDrug Resistance, NeoplasmFemaleHomeodomain ProteinsHumansHomeodomain ProteinsHOXC10 protein, human

Identifiers

PMID27302171
PMCPMC4970943
OpenAlexW2437775691

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.